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Article: Outcomes and Susceptibility to Neuraminidase Inhibitors in Individuals Infected with Different Influenza B Lineages: the Influenza Resistance Information Study.

TitleOutcomes and Susceptibility to Neuraminidase Inhibitors in Individuals Infected with Different Influenza B Lineages: the Influenza Resistance Information Study.
Authors
Keywordsantiviral
IC50
influenza B
lineage
neuraminidase inhibitor
Issue Date2016
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
The Journal of Infectious Diseases, 2016, v. 213 n. 2, p. 183-190 How to Cite?
AbstractBackground. Little is known about how influenza infections caused by B/Victoria and B/Yamagata virus lineages compare with respect to disease course and susceptibility to antiviral therapy. Methods. Data from patients with influenza B infections from the first 5 years (2009-2013) of the prospective Influenza Resistance Information Study (IRIS, NCT00884117) were evaluated. Cultured viruses were phenotypically tested for neuraminidase inhibitor (NAI) sensitivity, and sequenced to determine virus lineage (B/Victoria or B/Yamagata). Differences in clinical outcomes (viral clearance and symptom resolution) between virus lineages were assessed using Kaplan-Meier analysis. Results. In all, 914 patients were positive for influenza B by reverse transcriptase polymerase chain reaction (RT-PCR: B/Victoria, 586; B/Yamagata, 289; not subtyped, 39); 474 were treated with antivirals. No phenotypic resistance to oseltamivir or zanamivir was found in B/Victoria or B/Yamagata viruses. Of 15 predefined resistance mutations, 2 were detected by neuraminidase sequencing: I221T had reduced sensitivity to oseltamivir, and I221V was sensitive to NAI inhibition. No consistent differences between virus lineages in times to viral clearance or to symptom or fever resolution were found in adults and adolescents or in children. Conclusions. Influenza B virus lineage had no notable effect on disease outcomes or antiviral susceptibility in this population. © The Author 2015. Published by Oxford University Press for the Infectious Diseases Society of America.
Persistent Identifierhttp://hdl.handle.net/10722/211642
ISSN
2019 Impact Factor: 5.022
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorvan der Vries, E-
dc.contributor.authorIp, DKM-
dc.contributor.authorCowling, BJ-
dc.contributor.authorZhang, JD-
dc.contributor.authorTong, X-
dc.contributor.authorWojtowicz, K-
dc.contributor.authorSchutten, M-
dc.contributor.authorBoucher, CA-
dc.date.accessioned2015-07-21T02:06:29Z-
dc.date.available2015-07-21T02:06:29Z-
dc.date.issued2016-
dc.identifier.citationThe Journal of Infectious Diseases, 2016, v. 213 n. 2, p. 183-190-
dc.identifier.issn0022-1899-
dc.identifier.urihttp://hdl.handle.net/10722/211642-
dc.description.abstractBackground. Little is known about how influenza infections caused by B/Victoria and B/Yamagata virus lineages compare with respect to disease course and susceptibility to antiviral therapy. Methods. Data from patients with influenza B infections from the first 5 years (2009-2013) of the prospective Influenza Resistance Information Study (IRIS, NCT00884117) were evaluated. Cultured viruses were phenotypically tested for neuraminidase inhibitor (NAI) sensitivity, and sequenced to determine virus lineage (B/Victoria or B/Yamagata). Differences in clinical outcomes (viral clearance and symptom resolution) between virus lineages were assessed using Kaplan-Meier analysis. Results. In all, 914 patients were positive for influenza B by reverse transcriptase polymerase chain reaction (RT-PCR: B/Victoria, 586; B/Yamagata, 289; not subtyped, 39); 474 were treated with antivirals. No phenotypic resistance to oseltamivir or zanamivir was found in B/Victoria or B/Yamagata viruses. Of 15 predefined resistance mutations, 2 were detected by neuraminidase sequencing: I221T had reduced sensitivity to oseltamivir, and I221V was sensitive to NAI inhibition. No consistent differences between virus lineages in times to viral clearance or to symptom or fever resolution were found in adults and adolescents or in children. Conclusions. Influenza B virus lineage had no notable effect on disease outcomes or antiviral susceptibility in this population. © The Author 2015. Published by Oxford University Press for the Infectious Diseases Society of America.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org-
dc.relation.ispartofThe Journal of Infectious Diseases-
dc.rightsPre-print: Journal Title] ©: [year] [owner as specified on the article] Published by Oxford University Press [on behalf of xxxxxx]. All rights reserved. Pre-print (Once an article is published, preprint notice should be amended to): This is an electronic version of an article published in [include the complete citation information for the final version of the Article as published in the print edition of the Journal.] Post-print: This is a pre-copy-editing, author-produced PDF of an article accepted for publication in [insert journal title] following peer review. The definitive publisher-authenticated version [insert complete citation information here] is available online at: xxxxxxx [insert URL that the author will receive upon publication here].-
dc.subjectantiviral-
dc.subjectIC50-
dc.subjectinfluenza B-
dc.subjectlineage-
dc.subjectneuraminidase inhibitor-
dc.titleOutcomes and Susceptibility to Neuraminidase Inhibitors in Individuals Infected with Different Influenza B Lineages: the Influenza Resistance Information Study.-
dc.typeArticle-
dc.identifier.emailIp, DKM: dkmip@hku.hk-
dc.identifier.emailCowling, BJ: bcowling@hku.hk-
dc.identifier.authorityIp, DKM=rp00256-
dc.identifier.authorityCowling, BJ=rp01326-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/infdis/jiv375-
dc.identifier.pmid26160744-
dc.identifier.scopuseid_2-s2.0-84959883597-
dc.identifier.hkuros245573-
dc.identifier.volume213-
dc.identifier.issue2-
dc.identifier.spage183-
dc.identifier.epage190-
dc.identifier.isiWOS:000371237900004-
dc.publisher.placeUnited States-

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